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Id: biblio-1093610
Autor: Taboada Lugo, Noel.
Título: La vía de señalización Notch en el origen de algunas malformaciones congénitas / The Notch Signaling Pathway at the Origin of Some Congenital Malformations
Fonte: Rev. cuba. obstet. ginecol;44(3):1-17, jul.-set. 2018.
Idioma: es.
Resumo: La vía de señalización Notch desempeña un papel clave para regular el destino celular, crecimiento, proliferación y la muerte celular programada durante el desarrollo de organismos eucariotas. Esta vía está relacionada con una enorme diversidad de procesos del desarrollo y su disfunción está implicada en el origen de muchas malformaciones congénitas. Se realizó una revisión bibliográfica con el objetivo de actualizar la información sobre la vía de señalización Notch y su relación con el origen de diferentes malformaciones congénitas sensibles a la deficiencia materna de ácido fólico y otros micronutrientes. La literatura médica publicada en idiomas español e inglés se recopiló a través de buscadores como PubMed, Medline, Scielo, Lilacs y la biblioteca Cochrane en enero de 2018 usando palabras clave apropiadas. El conocimiento de esta vía de señalización podría ayudar a comprender mejor algunos aspectos de la morfogénesis, ya que, al actuar como un controlador maestro del destino celular, la proliferación, diferenciación y muerte celular programada, ofrece puntos específicos y susceptibles de intervención que posibilitan la prevención de determinadas malformaciones congénitas en el hombre(AU)

Notch signaling pathway plays a key role to regulate cell grow, fates, proliferation and programmed cell death in development of eukaryotic organisms. This pathway is related with an enormous diversity of developmental processes and its dysfunction is implicated in the origin of many congenital malformations. A review was performed to provide updated information on Notch signaling pathway involved in the origin of some congenital malformations related with maternal deficiency of folic acid and other micronutrients. Published medical literature in Spanish and English languages was retrieved from PubMed, Medline, Scielo, Lilacs and the Cochrane Library in January 2018, using appropriate key words. Knowledge about this signaling pathway could help to better understand some topics of morphogenesis, since by acting as a master controller of cell fate, proliferation, differentiation and programmed cell death, it offers susceptible and specific points which make possible to prevent some human congenital malformations(AU)
Descritores: Receptores Notch/análise
Receptores Notch/genética
Receptores Notch/uso terapêutico
Morfogênese/genética
-Anormalidades Congênitas/genética
Limites: Humanos
Tipo de Publ: Revisão
Responsável: CU1.1 - Biblioteca Médica Nacional


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Id: biblio-1089075
Autor: Zhu, Qing; Li, Jingchao; Wu, Qi; Cheng, Yongxia; Zheng, Huizhe; Zhan, Tao; Wang, Hongwei; Yang, Yue; Wang, Hongyan; Liu, Ye; Guo, Sufen.
Título: Linc-OIP5 in the breast cancer cells regulates angiogenesis of human umbilical vein endothelial cells through YAP1/Notch/NRP1 signaling circuit at a tumor microenvironment
Fonte: Biol. Res;53:05, 2020. tab, graf.
Idioma: en.
Projeto: Nature Science Foundation of Heilongjiang Province; . National Nature Science Foundation of China.
Resumo: BACKGROUND: LincRNAs have been revealed to be tightly associated with various tumorigeneses and cancer development, but the roles of specific lincRNA on tumor-related angiogenesis was hardly studied. Here, we aimed to investigate whether linc-OIP5 in breast cancer cells affects the angiogenesis of HUVECs and whether the linc-OIP5 regulations are involved in angiogenesis-related Notch and Hippo signaling pathways. METHODS: A trans-well system co-cultured HUVECs with linc-OIP5 knockdown breast cancer cell MDA-MB-231 was utilized to study the proliferation, migration and tube formation abilities of HUVECs and alterations of related signaling indicators in breast cancer cells and their conditioned medium through a series of cell and molecular experiments. RESULTS: Overexpressed linc-OIP5, YAP1, and JAG1 were found in breast cancer cell lines MCF7 and MDA-MB-231 and the expression levels of YAP1 and JAG1 were proportional to the breast cancer tissue grades. MDA-MB-231 cells with linc-OIP5 knockdown led to weakened proliferation, migration, and tube formation capacity of co-cultured HUVECs. Besides, linc-OIP5 knockdown in co-cultured MDA-MB-231 cells showed downregulated YAP1 and JAG1 expression, combined with a reduced JAG1 level in conditioned medium. Furthermore, a disrupted DLL4/Notch/NRP1 signaling in co-cultured HUVECs were also discovered under this condition. CONCLUSION: Hence, linc-OIP5 in MDA-MB-231 breast cancer cells may act on the upstream of the YAP1/Notch/NRP1 signaling circuit to affect proliferation, migration, and tube formation of co-cultured HUVECs in a non-cellular direct contact way through JAG1 in conditioned medium. These findings at least partially provide a new angiogenic signaling circuit in breast cancers and suggest linc-OIP5 could be considered as a therapeutic target in angiogenesis of breast cancers.
Descritores: Fatores de Transcrição/metabolismo
Neoplasias da Mama/patologia
Neuropilina-1/metabolismo
Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Receptores Notch/metabolismo
Microambiente Tumoral
Células Endoteliais da Veia Umbilical Humana/citologia
-Neoplasias da Mama/metabolismo
Imuno-Histoquímica
Transdução de Sinais
Western Blotting
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Linhagem Celular Tumoral
Reação em Cadeia da Polimerase em Tempo Real
Limites: Humanos
Feminino
Responsável: CL1.1 - Biblioteca Central


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Id: biblio-954937
Autor: Taboada Lugo, Noel; Herrera Martinez, Manuela.
Título: Mecanismos epigenéticos y vía de señalización Notch en el origen de diferentes defectos congénitos / Epigenetic mechanisms and Notch signalling pathway in the origin of different birth defects
Fonte: Medicentro (Villa Clara);22(3):197-207, jul.-set. 2018.
Idioma: es.
Descritores: Anormalidades Congênitas/genética
Receptores Notch
Epigenômica
Responsável: CU425.1 - Centro Provincial de Información de Ciencias Médicas de Villa Clara


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Id: lil-755036
Autor: Taha, Siti Aisyah Mohd; Ling, Joanne Koh Su; Azmi, Nur Izyan Binti; Kannan, Thirumulu Ponnuraj; Azlina, Ahmad; Mokhtar, Khairani Idah.
Título: Expression analysis of notsh signaling pathway molecules in shed cultured in keratinocyte growth medium
Fonte: Braz. j. oral sci;14(2):135-140, Apr.-June 2015. tab, ilus.
Idioma: en.
Projeto: Universiti Sains Malaysia Research.
Resumo: Aim: To detect the expression of molecules associated with Notch signaling pathway in stem cells from human exfoliated deciduous teeth (SHED) cultured in specific differentiation medium, namely, keratinocyte growth medium (KGM). Methods:RNA was extracted from SHED harvested on day 1, 3 and 7. RNA was reverse-transcribed to obtain the cDNA and then proceeded with PCR using specific primers for the Notch signaling pathway molecules (Notch1, Jagged-1, Jagged-2 and, Hes1) as well as stem cell marker (Nanog). PCR products were electrophoresed on a 2% agarose gel and stained with SYBR green. Results:Notch-1 was highly expressed in SHED cultured in KGM and showed increase in density as the days progressed, while Jagged-1 showed a decrease. Jagged-2 on the other hand, showed a slight increase on day 3 followed by a decrease on day 7. However, Hes-1 was not expressed in SHED cultured in KGM. Nanog showed expression only on day 3 and gradually increased in expression on day 7. Conclusions:Notch signaling pathway associated molecules; Notch-1, Jagged-1, Jagged-2, and stem cell marker Nanog are expressed in SHED cultured in KGM which may be involved in the differentiation into epithelial-like cells in human dental pulp tissues.
Descritores: Meios de Cultura
Dente Decíduo/citologia
Expressão Gênica
Queratinócitos
Receptores Notch
Células-Tronco
Limites: Humanos
Masculino
Feminino
Responsável: BR218.1 - Biblioteca Carlos Henrique Robertson Liberalli


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Id: lil-747156
Autor: Parajuli, Ramesh.
Título: Foreign Bodies in the Ear, Nose and Throat: An Experience in a Tertiary Care Hospital in Central Nepal
Fonte: Int. arch. otorhinolaryngol. (Impr.);19(2):121-123, Apr-Jun/2015.
Idioma: en.
Resumo: Introduction A foreign body (FB) is an object or substance foreign to the location where it is found. FBs in the ear, nose, and throat are a common problem frequently encountered in both children and adults. Objective To analyze FBs in terms of type, site, age, and gender distribution and method of removal. Methods A retrospective study was performed in a tertiary care hospital in the central part of Nepal. The study period was from June 2013 to May 2014. The information was obtained from hospital record books. Results A total of 134 patients had FBs in the ear, nose, or throat; 94 were males and 40 were females. Of the 134 patients, 70 (52.23% ) had FB in the ear, 28 (20.89% ) in the nose, and 36 (26.86% ) in the throat. The FB was animate (living) in 28 (40% ) patients with FB in the ear and 1 (3.5% ) patient with FB in the nose, but the FB was inanimate (nonliving) in any patient with FB in the throat, in 42 (60% ) patients with FB in the ear FB, and in 27 (96.4% ) patients with FB of the nose. The FB was removed with or without local anaesthesia (LA) in 98 (73.13% ) patients, and only 36 patients (26.86% ) required general anaesthesia (GA). The most common age group affected was <10 years. Conclusion FBs in the ear and nose were found more frequently in children, and the throat was the most common site of FB in adults and elderly people. Most of the FBs can be easily removed in emergency room or outpatient department. .
Descritores: Genes Supressores de Tumor/fisiologia
Oncogenes/fisiologia
Receptores Notch/fisiologia
-Eritrócitos/fisiologia
Genes de Troca
Neoplasias Hematológicas/tratamento farmacológico
Neoplasias Hematológicas/metabolismo
Hematopoese/genética
Células-Tronco Hematopoéticas/fisiologia
Megacariócitos/fisiologia
Transdução de Sinais/fisiologia
Limites: Animais
Humanos
Tipo de Publ: Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Revisão
Responsável: BR1.1 - BIREME


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Id: lil-717081
Autor: Carbonell Medina, Belfran Alcides.
Título: Rol de la vía de señalización notch durante el desarrollo de estructuras craneofaciales / The role of notch signaling pathway in the development of craniofacial structures
Fonte: Rev. Fac. Odontol. Univ. Antioq;26(1):164-179, jul.-dic. 2014. ilus, tab.
Idioma: es.
Resumo: La vía de señalización NOTCH es un mecanismo de señalización célula-célula conservado evolutivamente entre las especies, el cual es indispensable para un correcto desarrollo embrionario, mediando una variedad de procesos celulares como proliferación, diferenciación, apoptosis, transformación epitelio- mesénquimal, migración, angiogénesis, mantenimiento de células madre y definición de destino celular. Varios genes componentes de esta vía han sido implicados en el desarrollo de estructuras craneofaciales. El 80% de los pacientes con síndrome de Alagille, presentan mutaciones en el gen que codifica para el receptor Jagged1 (Jag1), acompañado de hipoplasia del tercio medio facial y de craneosinostosis esporádica. Ratones con mutaciones homocigotas en el gen Jagged2 (Jag2) presentan paladar hendido, como resultado de fusiones ectópicas entre la lengua y los procesos palatinos. Por otro lado, mutaciones inducidas en el gen Hes1 generan defectos en el desarrollo de estructuras craneofaciales, derivadas de las células de la cresta neural craneal (CCNC) que incluyen: paladar hendido, agenesia del hueso frontal, malformación de base craneal y disminución en el tamaño del maxilar superior e inferior. Recientes estudios han evidenciado alteraciones durante la morfogénesis dental de ratones mutantes Jagged2-/-, acompañada de defectos en la citodiferenciación de ameloblastos y deficiente deposición de matriz de esmalte. Estos estudios muestran cómo la vía de señalización NOTCH está implicada en el desarrollo de una variedad de estructuras craneofaciales como paladar, dientes, maxilares y cráneo. Por esta razón, el propósito del presente artículo es presentar una revisión de las diferentes funciones de la vía NOTCH durante el desarrollo de estas estructuras craneofaciales, y de las alteraciones resultantes cuando existen mutaciones en algunos genes componentes de la vía NOTCH, como Jagged2, Jagged1, Hes1, Notch1 y Notch2.
Descritores: Receptores Notch
Tipo de Publ: Revisão
Responsável: CO66.1 - Biblioteca


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Id: lil-697677
Autor: Zhou, X.L.; Liu, J.C..
Título: Role of Notch signaling in the mammalian heart
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;47(1):1-10, 01/2014. tab, graf.
Idioma: en.
Projeto: the National Natural Science Foundation of China; . the Natural Science Foundation of Jiangxi Province; . the Graduate Innovation Fund of Jiangxi Province.
Resumo: Notch signaling is an evolutionarily ancient, highly conserved pathway important for deciding cell fate, cellular development, differentiation, proliferation, apoptosis, adhesion, and epithelial-to-mesenchymal transition. Notch signaling is also critical in mammalian cardiogenesis, as mutations in this signaling pathway are linked to human congenital heart disease. Furthermore, Notch signaling can repair myocardial injury by promoting myocardial regeneration, protecting ischemic myocardium, inducing angiogenesis, and negatively regulating cardiac fibroblast-myofibroblast transformation. This review provides an update on the known roles of Notch signaling in the mammalian heart. The goal is to assist in developing strategies to influence Notch signaling and optimize myocardial injury repair.
Descritores: Cardiopatias/metabolismo
Miocárdio/metabolismo
Receptores Notch/metabolismo
Transdução de Sinais/fisiologia
-Apoptose/fisiologia
Diferenciação Celular/fisiologia
Cardiopatias/fisiopatologia
Precondicionamento Isquêmico Miocárdico
Mamíferos
Regeneração/fisiologia
Limites: Animais
Humanos
Tipo de Publ: Research Support, Non-U.S. Gov't
Revisão
Responsável: BR1.1 - BIREME


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Id: lil-591861
Autor: Glavic, Alvaro; López-Varea, Ana; de Celis, José F.
Título: The balance between GMD and OFUT1 regulates Notch signaling pathway activity by modulating Notch stability
Fonte: Biol. Res;44(1):25-34, 2011. ilus.
Idioma: en.
Projeto: ICM; . BFU.
Resumo: The Notch signaling pathway plays an important role in development and physiology. In Drosophila, Notch is activated by its Delta or Serrate ligands, depending in part on the sugar modifications present in its extracellular domain. O-fucosyltransferase-1 (OFUT1) performs the first glycosylation step in this process, O-fucosylating various EGF repeats at the Notch extracellular domain. Besides its O-fucosyltransferase activity, OFUT1 also behaves as a chaperone during Notch synthesis and is able to down regulate Notch by enhancing its endocytosis and degradation. We have reevaluated the roles that O-fucosylation and the synthesis of GDP-fucose play in the regulation of Notch protein stability. Using mutants and the UAS/Gal4 system, we modified in developing tissues the amount of GDP-mannose-deshydratase (GMD), the first enzyme in the synthesis of GDP-fucose. Our results show that GMD activity, and likely the levels of GDP-fucose and O-fucosylation, are essential to stabilize the Notch protein. Notch degradation observed under low GMD expression is absolutely dependent on OFUT1 and this is also observed in Notch Abruptex mutants, which have mutations in some potential O-fucosylated EGF domains. We propose that the GDP-fucose/OFUT1 balance determines the ability of OFUT1 to endocytose and degrade Notch in a manner that is independent of the residues affected by Abruptex mutations in Notch EGF domains.
Descritores: Proteínas de Drosophila/metabolismo
Drosophila melanogaster/genética
Fucosiltransferases/metabolismo
Guanosina Difosfato Fucose/metabolismo
Guanosina Difosfato Manose/metabolismo
Receptores Notch/metabolismo
Asas de Animais/metabolismo
-Alelos
Proteínas de Drosophila/genética
Drosophila melanogaster/anatomia & histologia
Drosophila melanogaster/metabolismo
Endocitose/genética
Fucosiltransferases/genética
Guanosina Difosfato Fucose/genética
Guanosina Difosfato Manose/genética
Imuno-Histoquímica
Hibridização In Situ
Peptídeos e Proteínas de Sinalização Intracelular/genética
Proteínas Mutantes/genética
Proteínas Mutantes/metabolismo
Mutação/genética
Fenótipo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Receptores Notch/genética
Transdução de Sinais
Asas de Animais/anatomia & histologia
Limites: Animais
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


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Id: lil-520063
Autor: Rozante, L. C. S; Gubitoso, M. D; Matioli, S. R.
Título: A framework for modeling of juxtacrine signaling systems
Fonte: Genet. mol. res. (Online);6(4):821-845, 2007. ilus.
Idioma: en.
Conferência: Apresentado em: X-Meeting 2006 - International Conference of the AB3C, 2, Apresentado em: Annual International Conference on Intelligent Systems for Molecular Biology, 14, Fortaleza, Aug. 6-10, 2006.
Resumo: Juxtacrine signaling is intercellular communication, in which the receptor of the signal (typically a protein) as well as the ligand (also typically a protein, responsible for the activation of the receptor) are anchored in the plasma membranes, so that in this type of signaling the activation of the receptor depends on direct contact between the membranes of the cells involved. Juxtacrine signaling is present in many important cellular events of several organisms, especially in the development process. We propose a generic formal model (a modeling framework) for juxtacrine signaling systems that is a class of discrete dynamic systems. It possesses desirable characteristics in a good modeling framework, such as: a) structural similarity with biological models, b) capacity of operating in different scales of time, and c) capacity of explicitly treating both the events and molecular elements that occur in the membrane, and those that occur in the intracellular environment and that are involved in the juxtacrine signaling process. We have implemented this framework and used it to develop a new three-level discrete model for the neurogenic network and its participation in neuroblast segregation. This paper presents the details of this framework and its current status.
Descritores: Modelos Biológicos
Proteínas de Drosophila/metabolismo
RNA Mensageiro/genética
Software
Transdução de Sinais
-Células-Tronco/citologia
Drosophila melanogaster/citologia
Drosophila melanogaster/embriologia
Drosophila melanogaster/metabolismo
Neurônios/citologia
Organogênese
RNA Mensageiro/metabolismo
Receptores Notch/metabolismo
Limites: Animais
Responsável: BR26.1 - Biblioteca Central


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Id: lil-495215
Autor: Vaglio, Alicia; Ferreira, Marnels; Panuncio, Ana Luisa; Castagnola, María Antonia; Pebet, Matías; De la Peña, Soledad; Quadrelli, Roberto.
Título: CADASIL: comunicación de una familiauruguaya con definición clínica, imagenológica, anatomopatológica y genética molecular / Clinical, imagenology, anatomopathological and molecular genetics results for the diagnosis of CADASIL in a Uruguayan family
Fonte: Rev. méd. Urug;24(1):24-31, mar. 2008. ilus, tab.
Idioma: es.
Resumo: Introducción: el síndrome CADASIL (Cerebral Dominant Arteriopathy with Subcortical Infarcts and Leukoencephlopathy) es una microangiopatía no amiloidea, no ateromatosa que se transmite en forma autosómica dominante y cuyas principales manifestaciones clínicasocurren a nivel cerebral. Su diagnóstico requiere criterios clínicos, imagenológicos y genéticos moleculares.Material y método: se estudiaron anatomopatológicamente mediante biopsia de piel y músculo y estudio genético molecular a tres integrantes de una familia con diagnóstico de CADASIL.Resultados: los exámenes clínicos, paraclínicos, neurológicos y ultraestructural de biopsia de piel mostraron resultados consistentes con CADASIL. La secuenciación de exones 2,3,4,5,8,11,20,23 del gene NOTCH3 detectó una mutación en forma heterocigota en el exón 5 no descripta en la literatura.Conclusiones: destacamos la importancia del diagnóstico precoz de esta enfermedad y la definición molecular que permite el asesoramiento genético a todos los integrantes de lafamilia y, eventualmente, el diagnóstico prenatal.

Introduction: CADASIL syndrome (Cerebral Dominant Arteriopathy with Subcortical Infarcts and Leukoencephlopathy),the most common form of hereditary stroke disorder is a nonamyloid, non-atheromatous microangiopathy. Main clinical features are found in the brain. The disease may be diagnosed by clinical findings, images and geneticmolecular criteria.Methods: an anatomopathological analysis through a skin and muscle biopsy and molecular study was performed on three members of the same family diagnosed with CADASIL.Results: clinical, paraclinical, neurological and ultrastructuralskin biopsy study's findings were consistent with CADASIL. NOTCH3 sequence exonal analysis(2,3,4,5,8,11,20,23) suggested heterocigotic mutations in exon 5, not previously described in literature.Conclusions: we stress the importance of early diagnosis of this disease and the molecular definition that enablesgenetic counselling to all members of the family and, potentially, prenatal diagnosis of the disease.

Introdução: a síndrome CADASIL (Cerebral Dominant Arteriopathy with Subcortical Infarcts and Leukoencephlopathy)é uma microangiopatia não amiloidea, não ateromatosa que se transmite de maneira autossômica dominantecujas principais manifestações clinicas são observadas no cérebro. Para seu diagnóstico é necessário realizarprovas clínicas, imagenológicas e de genética molecular.Material e método: foram realizados exames de anatomia patológica e de genética molecular em biopsias depele e músculo a três integrantes de uma família com diagnóstico de CADASIL.Resultados: os exames clínicos, paraclínicos, neurológicos e ultra-estrutural da biopsia de pele mostraram resultados consistentes com CADASIL. A seqüenciação dos exons 2,3,4,5,8,11,20,23 do gene NOTCH3 detectou uma mutação em forma heterozigótica no exon 5 não descritana literatura.Conclusões: destacamos a importância do diagnóstico precoce desta doença e a definição molecular que permite o assessoramento genético a todos os integrantes da família e, eventualmente, o diagnóstico pré-natal.
Descritores: CADASIL
Mutação/genética
Receptores Notch/genética
Responsável: UY6.1 - Biblioteca



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